Inhibition of reactive oxygen species production accompanying alternatively activated microglia by risperidone in a mouse ketamine model of schizophrenia.
Journal of neurochemistry September 1, 2024 Risako Fujikawa, Jun Yamada, Shoichiro Maeda et al. 6 citations
In a mouse model of schizophrenia, the antipsychotic risperidone reduced behavioral abnormalities and altered microglial activity and reactive oxygen species (ROS) in the hippocampus. Mice given ketamine showed schizophrenia-like behaviors, increased microglial density, and a shift toward more activated microglial shapes. Risperidone reversed these changes, lowering expression of the ROS-producing enzyme Nox2 and raising antioxidant enzyme levels. In isolated microglia, ketamine boosted ROS production, which risperidone blocked. A NOX2 inhibitor also counteracted ketamine-induced behavioral deficits, suggesting that reducing ROS via microglial modulation may help treat schizophrenia.